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CLINICAL PHARMACOLOGICAL FEATURES OF RATIONAL USE OF DRUGS IN
THROMBOEMBOLIC SYNDROME
¹Omonova Guzal Zarifovna
²Jurayev Shahzod Zokirovich
³Quchqorov Bahodir Uvaydulla o'g'li
¹Assistant Professor, Department of Clinical Pharmacology, Samarkand State Medical
University.
²'³Students of Samarkand State Medical University.
https://doi.org/10.5281/zenodo.14804184
Abstract.
All pulmonary embolisms are small, physiologically insignificant, and
asymptomatic. When symptoms are present, they are nonspecific and vary in frequency and
intensity depending on the degree of pulmonary artery occlusion and the underlying heart and
lung status. A second heart sound (S2) may be present due to an increase in the pulmonary
component (P2), but is uncommon in acute PE because the increase in pulmonary artery pressure
is modest. Wheezing or rales may occur, but these sounds are usually related to underlying medical
conditions. In the presence of right ventricular failure, there is dilatation of the internal jugular
veins and right ventricular distention, a gallop rhythm is heard (appearance of the third heart
sound [S3]), and a murmur of tricuspid regurgitation may be heard.
Keywords:
Embolism, Acute shortness of breath, Pleuritic chest pain (pulmonary
infarction), Tachycardia, Tachypnea.
INTRODUCTION
Chronic thromboembolic pulmonary hypertension leads to right ventricular failure, which
manifests as shortness of breath during physical exertion, fatigue, and peripheral edema that
develops over months or years.
Patients with acute pulmonary embolism may also have signs of deep vein thrombosis (i.e.,
pain, swelling, and/or erythema of the lower or upper extremities). However, patients often do not
have such signs in their lower legs.
a.
Diagnosis of pulmonary embolism
b.
High level of suspicion of the presence of the disease
c.
Pre-examination probability assessment (based on clinical presentation, including pulse
oximetry and chest X-ray)
d.
Follow-up investigation based on probability assessment
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The diagnosis of pulmonary embolism is difficult because the presenting complaints and
symptoms are nonspecific and diagnostic tests are not 100% sensitive and specific. PE should be
considered in the differential diagnosis if nonspecific symptoms such as shortness of breath,
pleuritic pain, hemoptysis, dizziness, or syncope are present. Thus, PE should be considered in the
differential diagnosis of patients with suspected:
Глава 1
Myocardial ischemia;
Глава 2
Heart failure
Глава 3
Exacerbation of chronic obstructive pulmonary disease (COPD)
Глава 4
Pneumothorax
Глава 5
Zatiljam
Глава 6
Sepsis
Глава 7
Acute chest syndrome (in patients with sickle cell anemia);
Глава 8
Acute anxiety with hyperventilation
The diagnostic sign may be clinically significant tachycardia of unknown etiology.
Pulmonary embolism should be suspected in any elderly person with tachypnea and altered mental
status.
Pulse oximetry and chest X-ray are used as initial diagnostic methods. ECG, arterial blood
gas measurements, or both can help rule out other diagnoses (e.g., acute myocardial infarction).
RESEARCH METHODS AND APPROACHES
Chest radiography is usually unremarkable but may reveal atelectasis, focal infiltrates,
hemispheric elevation, or pleural effusion.
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Classic findings such as focal absence of lung signs (Westermarck sign), peripheral wedge-
shaped pleural shadow (Hampton's mound), or dilation of the right descending pulmonary artery
suggest PE but are rare and therefore have limited sensitivity and specificity. Chest radiography
can also rule out pneumonia. Pulmonary infarction due to pulmonary embolism may be mistaken
for pneumonia.
Almost all pulmonary embolisms are caused by blood clots in the veins of the legs or pelvis
(deep vein thrombosis). The risk of embolization is increased if the clot is located in the popliteal
vein or higher. Thromboembolism can also occur in the veins of the arms or in the central veins of
the chest (which occur when central venous catheters are used or as a result of thoracic outlet
syndrome).
Pulmonary embolism can also arise from nonthrombotic sources (e.g., air embolism,
amniotic fluid, fat, infected material, orthopedic cement, foreign div, tumor).
Risk factors for deep vein thrombosis and pulmonary embolism (see table Risk factors for
deep vein thrombosis and pulmonary embolism) are similar in children and adults and include:
Conditions that impair venous outflow, including bed rest and hospitalization without
ambulation;
Conditions that cause endothelial damage or dysfunction, such as trauma or surgery
Hypercoagulable (thrombophilic) diseases, such as cancer or primary blood clotting
disorders
COVID-19 is a risk factor for the development of deep vein thrombosis and pulmonary
embolism. Although part of the risk is related to the decreased mobility associated with the disease,
SARS-CoV-2 infection may induce prothrombotic changes.
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Pathophysiology of pulmonary embolism
Once deep vein thrombosis occurs, the clots can break off and travel through the venous
system, traveling to the right side of the heart and then to the pulmonary arteries, partially or
completely blocking one or more vessels. Outcomes depend on the size and number of emboli, the
initial condition of the lungs, the ability of the div's thrombolytic system to dissolve the clots,
and how well the right ventricle (RV) is functioning. Death, when it occurs, is often due to right
ventricular failure.
Small emboli do not have an immediate effect; most begin to disintegrate and dissolve
within hours or days. Large emboli can cause reflex increased pulmonary ventilation (tachypnea),
hypoxemia due to ventilation-perfusion mismatch, low venous oxygen content due to decreased
cardiac output, atelectasis due to alveolar hypocapnia and abnormal surfactant, and increased
pulmonary vascular resistance, leading to mechanical obstruction and vasoconstriction,
tachycardia, and hypotension. Most thrombi, even of moderate size, dissolve by endogenous lysis,
a physiological effect that gradually disappears over hours or days. Some emboli are resistant to
lysis and can form and persist, sometimes causing chronic thromboembolic pulmonary
hypertension (CTEPH).
RESEARCH RESULTS
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Pulmonary embolism can be classified according to the physiological effects described by
the European Society of Cardiology/American Heart Association ( 1 ):
High risk (massive): Right ventricular dysfunction leading to hypotension, defined as
systolic blood pressure < 90 mmHg. Art. or a decrease in systolic blood pressure ≥ 40 mm Hg. Art.
within 15 minutes from baseline
Intermediate risk (submassive): Right ventricular dysfunction without hypotension. This is
evidenced by right ventricular dilatation and/or hypokinesia on imaging (e.g., CT angiography,
echocardiography) and elevated circulating biomarkers (e.g., troponin, brain natriuretic peptide).
It is important to note that the European Society of Cardiology also considers a patient to have
intermediate risk pulmonary embolism if the simplified pulmonary embolism severity index
(sPESI) is > 0, including patients with other comorbidities or symptoms ( 1 ). Intermediate-risk
pulmonary embolism can be divided into intermediate-high risk (presence of right ventricular
dysfunction on imaging and elevation of circulating biomarkers) and intermediate-low risk
(presence of right ventricular dysfunction on imaging or elevation of circulating biomarkers).
Low risk: no right ventricular failure and hypotension (sPESI score = 0 according to the
European Society of Cardiology)
Saddle pulmonary embolism is a pulmonary embolism that occurs in the area of the main
pulmonary artery and the bifurcation of the right and left pulmonary arteries; Saddle embolism is
usually, but not always, considered to be of intermediate or high risk. The saddle configuration
does not require a specific therapeutic approach. Although saddle emboli are often large and cause
near-total or complete obstruction, they can also be relatively small, non-obstructive emboli.
In 1-3% of cases, chronic residual obstruction leads to pulmonary hypertension (chronic
thromboembolic pulmonary hypertension), which develops over several months to years and can
lead to chronic right ventricular failure.
In cases of acute occlusion of the major pulmonary arteries by large emboli or in cases
where a cluster of multiple small emboli occludes a significant portion of the more distal vessels,
RV pressure increases, which can lead to acute RV failure, shock, or sudden death. The risk of
death depends on the degree and rate of rise in right-sided pressure and the patient's initial
cardiopulmonary status. Patients with pre-existing cardiopulmonary disease are at increased risk
of death, but younger and/or generally healthy patients may survive PE with more than 50%
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Pulmonary infarction (interruption of blood flow in a pulmonary artery, resulting in
ischemia of lung tissue, sometimes pleurally based [peripherally located], often as a wedge-shaped
shadow on chest radiography [Hampton's hill] or other imaging studies) occurs in < 10% of
patients diagnosed with PE. This low rate is associated with a bilateral blood supply to the lung
(i.e., from the bronchial and pulmonary arteries). Pulmonary infarction usually results from small
emboli that occlude more distal pulmonary arteries and is almost always reversible; pulmonary
infarction is recognized early, often before necrosis occurs.
Pulse oximetry is a convenient and rapid method for assessing oxygenation; hypoxemia is
often present in PE and requires further investigation. In patients with dyspnea or tachypnea, blood
gas analysis, especially pulse oximetry, may not detect hypoxia. Arterial blood gas measurements
may reveal an increased alveolar-arterial oxygen (Aa) gradient (sometimes called the "Aa
gradient") or hypocapnia. Pulse oximetry and blood gas measurements are moderately sensitive
but not specific for PE. Oxygen saturation may be normal due to a small thrombus load or
compensatory hyperventilation; a very low partial pressure of carbon dioxide (PCO2) measured
by arterial blood gas measurements may confirm hyperventilation.
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The ECG often shows tachycardia and various changes in the terminal part of the
ventricular ST-T complex that are not typical of pulmonary embolism (see ECG picture in
pulmonary embolism). The appearance of S1Q3T3 (S wave in lead I, Q wave in lead III, inverted
T wave in lead III) or right bundle branch block may indicate severe right ventricular dilatation
affecting the conduction pathways. These findings are highly specific but not sensitive and occur
in only 5% of patients, although they are found in the majority of patients with massive PE. Right
axis deviation may be detected (R > S in V1). T wave inversion may also be present in leads V1-
V4.
a.
ECG for pulmonary embolism
b.
The ECG shows sinus tachycardia with a heart rate of 110 beats per minute, S1Q3T3, and
an R wave = S wave in lead V1 in a patient with established PE.
c.
ECG for pulmonary embolism
d.
Clinical calculator
e.
Alveolar-arterial gradient
The clinical probability of PE can be assessed by analyzing ECG and chest X-ray data in
conjunction with anamnestic data and physical examination findings. Clinical prognostic scores,
such as the Wells score or the revised Geneva score ( 1 ) or the pulmonary embolism exclusion
criteria (PERC), help clinicians assess the likelihood of developing acute pulmonary embolism.
These initial scores for various clinical factors, combined with the scores, correspond to
pretest probability markers for PE (pretest probability). For example, the Wells score for PE is
classified as probable or unlikely. Clinical probability assessment has been best studied in patients
presenting to the emergency department.
One of the most important clinical criteria is the assumption that PE is more likely than
another disease, an assumption that is highly subjective. In addition, the clinical judgment of
experienced clinicians may be as sensitive or even more sensitive than the results of such scales.
If at least one complaint or symptom, in particular dyspnea, hemoptysis, tachycardia, or
hypoxemia, has no clear cause on the basis of clinical or radiological data, the diagnosis of PE is
more likely.
Clinical probability indices guide investigation strategies and interpretation of study results.
For patients at low risk of developing PE, only minimal additional testing is required (i.e.,
outpatient D-dimer testing). In such cases, a negative D-dimer test (< 0.4 μg/mL [< 2.2 nmol/L])
is highly suggestive of the absence of pulmonary embolism. If there is a high clinical suspicion for
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PE and the risk of bleeding is low, anticoagulants should be considered immediately until the
diagnosis is confirmed by further testing.
The rule of exclusion for pulmonary embolism defines 8 criteria. The presence of all of
these criteria in a patient considered to be at low risk based on clinical data indicates that testing
for PE is not indicated ( 2 ). These criteria are:
1.
Age < 50 years
2.
Heart rate <100
3.
Oxygen saturation ≥ 95%
4.
No prior deep vein thrombosis or pulmonary embolism
5.
Absence of unilateral leg swelling
6.
Estrogen is not taken
7.
No hemoptysis
8.
No history of surgery or injury requiring hospitalization within the past 4 weeks
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The use of pulmonary embolism exclusion criteria (PERC) has been proposed as a way to
reduce the rate of PE testing compared with the traditional D-dimer test, but has similar sensitivity
and negative predictive values.
Diagnostic research
Screen outpatients with D-dimer testing if the initial study probability assessment indicated
a low or moderate probability;
If there is a high probability of thromboembolism before the test or if D-dimer
concentrations are elevated, CT angiography is performed, or ventilation-perfusion (V/Q)
scintigraphy is performed if renal failure is present when CT contrast is contraindicated.
Sometimes - ultrasound of the legs or arms (to confirm deep vein thrombosis if there is a
delay in lung imaging or contraindications)
1.
There is no universal algorithm for suspecting pulmonary embolism. The most useful tests
to diagnose or rule out PE are:
2.
D-dimer detection
3.
CT angiography
4.
Ventilation-perfusion lung scintigraphy
5.
Doppler ultrasound examination
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Echocardiography may be useful in detecting pulmonary embolism (a migrating thrombus)
en route to the lungs or in detecting new signs of right ventricular dysfunction. Echocardiographic
signs that may indicate pulmonary embolism include the 60/60 sign, which is a pulmonary artery
acceleration time of <60 milliseconds and a peak systolic tricuspid gradient of <60 mmHg. Art.
( 3 ), and the McConnell sign, which is a decrease in the contractility of the RV free wall relative
to the RV peak ( 4 ).
D-dimer is produced by fibrinolysis; its elevation is associated with recent thrombosis.
Traditionally, if the pretest probability is considered low or intermediate, a negative D-dimer level
(< 0.4 μg/mL [< 2.2 nmol/L]) is a highly sensitive indicator of the absence of PE with a negative
predictive value of > 95%; in most cases, this result is reliable enough to rule out PE in the
emergency department or clinic setting. Recent data have shown that D-dimer levels may increase
with age, which may lead to false-positive test results. Therefore, in patients older than 50 years
with a low or intermediate pretest probability of PE, the most common adjustment factor is to use
the age cutoff in ng/mL multiplied by 10. However, elevated D-dimer levels are not specific for
venous thromboembolism, as many patients without deep vein thrombosis (DVT) or PE also have
elevated levels (especially hospitalized patients). Therefore, if D-dimer levels are elevated or if
there is a high initial probability of PE, further investigation is warranted.
CT angiography is the preferred method for the diagnosis of acute PE. It is rapid, accurate,
highly sensitive, and specific. It provides more information about other pulmonary pathologies
(e.g., pneumonia to rule out PE as a cause of chest pain due to hypoxia or pleurisy) and also allows
for assessment of the severity of PE (e.g., lung volume, right ventricular or hepatic venous reflux).
Although poor scan quality due to motion artifacts or poor bolus contrast enhancement can limit
the sensitivity of the study, CT technology now allows for relatively still images in dyspneic
patients, reducing data acquisition times to < 2 s. Fast scan times allow for the use of small volumes
of iodinated contrast material, which reduces the risk of developing acute renal failure.
CONCLUSION
The sensitivity of CT angiography in PE is highest in the main pulmonary artery or in lobar
or segmental branches. The sensitivity of CT angiography is low in detecting emboli in
subsegmental vessels (approximately 30% of all pulmonary emboli). However, unless
contraindicated, CT angiography remains the preferred modality for diagnosing acute PE.
In pulmonary embolism, ventilation/perfusion scintigraphy identifies areas of the lung that
are ventilated but not perfused. Ventilation-perfusion scintigraphy is more time-consuming and
less specific than CT angiography. However, this test is highly sensitive if the chest radiograph is
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normal or near normal and there is no underlying lung disease. V/Q scanning is particularly
informative in patients with renal failure that precludes the use of contrast agents, which are
required for CT angiography, and in pregnant women ( 5 ). In some hospitals, V/Q scintigraphy
can be performed using a portable machine that provides 3-dimensional images of ventilation and
perfusion, which is useful when the patient is too weak to move. Perfusion defects can also be seen
in many other lung diseases (eg, COPD, pneumosclerosis, pneumonia, pleural effusion).
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